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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

Ataxia telangiectasia mutated homolog

serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: p53, CAN, p21, V1a, HAD
Papers on Atm
The Rad50 hook domain regulates DNA damage signaling and tumorigenesis.
Petrini et al., New York City, United States. In Genes Dev, Apr 2014
These outcomes were dependent on ATM, as all phenotypes were mitigated in Rad50(+/46) Atm(+/-) mice.
EZH2-mediated H3K27 trimethylation mediates neurodegeneration in ataxia-telangiectasia.
Herrup et al., United States. In Nat Neurosci, Dec 2013
The symptoms of ataxia-telangiectasia (A-T) include a progressive neurodegeneration caused by ATM protein deficiency.
The epithelium specific cell cycle regulator 14-3-3sigma is required for preventing entry into mitosis following ultraviolet B.
Herzinger et al., München, Germany. In Photodermatol Photoimmunol Photomed, Dec 2013
METHODS: Cell lines expressing a dominant negative mutant of ataxia telangiectasia and Rad3 related (Atr) protein or overexpressing Cdc25A, cells deficient for 14-3-3σ, Nijmegen breakage syndrome (Nbs), or Ataxia telangiectasia mutated (Atm) were treated with ultraviolet B (UVB) and harvested after 12 h, 24 h, or 48 h for analysis by flow cytometry.
R-loops in proliferating cells but not in the brain: implications for AOA2 and other autosomal recessive ataxias.
Lavin et al., Brisbane, Australia. In Plos One, Dec 2013
There was no evidence for accumulation of R-loops in the brains of mice where Setx, Atm, Tdp1 or Aptx genes were disrupted.
Anthracyclines induce DNA damage response-mediated protection against severe sepsis.
Moita et al., Lisbon, Portugal. In Immunity, Dec 2013
This salutary effect is strictly dependent on the activation of DNA damage response and autophagy pathways in the lung, as demonstrated by deletion of the ataxia telangiectasia mutated (Atm) or the autophagy-related protein 7 (Atg7) specifically in this organ.
Expression pattern of ataxia telangiectasia mutated (ATM), p53, Akt, and glycogen synthase kinase-3β in the striatum of rats treated with 3-nitropropionic acid.
Pelegrí et al., Barcelona, Spain. In J Neurosci Res, 2012
We examined whether cellular expression of ataxia telangiectasia mutated, p53, Akt, and glycogen synthase kinase-3beta, were involved in the striatal neurodegeneration in the brains of rats
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
Kubota et al., Tokyo, Japan. In Nat Med, 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
Herrup et al., United States. In Nat Med, 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
ATM controls meiotic double-strand-break formation.
Keeney et al., New York City, United States. In Nature, 2011
Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair.
Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.
Burn et al., Sioux Falls, United States. In Drug Discov Today, 2011
The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cell-cycle progression.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Pearson et al., Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
Mdm2 links genotoxic stress and metabolism to p53.
Li et al., Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Li et al., Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
Hall et al., New York City, United States. In Adv Space Res, 2010
We investigated the role of heterozygosity for Atm, Rad9 and Brca1 on cell oncogenic transformation and cell survival induced by 1GeV/n (56)Fe ions.
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
Camins et al., Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
Frisan et al., Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
Chapple et al., London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?
Sunnerhagen et al., Göteborg, Sweden. In Mol Microbiol, 2008
In Schizosaccharomyces pombe, the Ataxia Telangiectasia-mutated (Atm)/Atm and Rad 3 Related (Atr) homologue Rad3 is an essential regulator of the response to DNA damage and stalled replication forks.
ATM activation and DNA damage response.
Kozlov et al., Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.
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